The goal of this research is to characterize the mechanism of ErR in campylobacters and clone the gene responsible. The working hypotheses are 1) that ErR is mediated by an rRNA methylase, the most common cause of ErR in gram positive organisms, 2) that the ErR gene in campylobacter can be cloned and expressed in E. coli using standard techniques, and 3) this gene will be inducible with other antimicrobials commonly found in animal feeds. The mechanisms of resistance will be investigated by examining the binding of labeled erythromycin to ribosomes prepared from sensitive and resistant strains of campylobacter. Permeability and drug inactivation studies will be carried out if no evidence for an rRNA methylase is discovered. A cosmid library of genomic DNA will be developed from ErR strains and expressed in E. coli. In the absence of expression, attempts will be made to clone the gene in campylobacter or streptococcal hosts. The cloned gene will be characterized by restriction endonuclease mapping, transposon mutagenesis and the nucleotide sequence determined. This research will attempt to prove that the genes for ErR in campylobacter arose in gram positive organisms and were transferred into campylobacter in vivo, and that antimicrobials commonly used in animal feeds can induce the ErR phenotype.